ArticleJournal of thoracic disease2026
Macrophage-enriched HMOX1 is an ischemia-reperfusion-responsive marker in the heart.
Article in Journal of thoracic disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Myocardial ischemia-reperfusion (I/R) injury triggers rapid innate immune activation, yet cell-type-resolved, I/R-responsive markers that bridge macrophage biology and translational relevance remain insufficiently defined. This study aimed to identify cell-type-resolved I/R-responsive markers in the heart and to clarify the translational relevance of macrophage-enriched HMOX1 in myocardial ischemia-reperfusion injury. Methods: A murine bulk myocardial transcriptomic dataset (GSE160516, spanning 6, 24, and 72 h post-reperfusion time points) was analyzed using differential expression and weighted gene co-expression network analysis (WGCNA), followed by functional enrichment and protein-protein interaction analyses. Candidate genes were prioritized through interpretable feature-selection models [least absolute shrinkage and selection operator (LASSO) regression and shapley additive explanations (SHAP)-based random forest analysis]. Cell-type specificity was resolved in an independent single-cell RNA-sequencing dataset (GSE288103). The top-ranked candidate was subsequently validated in a rat myocardial I/R model using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Complementary human genetic colocalization and in silico docking analyses were conducted as exploratory, hypothesis-generating exercises. Results: An I/R-associated co-expression module was enriched for immune and inflammatory pathways. Across multiple prioritization strategies, HMOX1 consistently ranked among the leading candidates. In bulk data, HMOX1 correlated with macrophage-related signals, and single-cell analysis confirmed predominant expression in macrophages. RT-qPCR demonstrated elevated myocardial HMOX1 transcript levels in rats following I/R. An independent external bulk RNA-seq cohort (GSE225105) showed a directionally concordant increase in HMOX1 expression, although this did not reach statistical significance in the limited sample. Colocalization and docking analyses yielded preliminary, hypothesis-generating signals. Conclusions: Integrated bulk and single-cell transcriptomic analyses, together with cross-species RT-qPCR validation, identify HMOX1 as a macrophage-enriched, I/R-responsive marker. These findings delineate a tractable candidate for future mechanistic studies investigating macrophage-associated responses in myocardial I/R injury.
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